Catalyst Athletics Forums - Heart Mass Gain

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- - Heart Mass Gain (http://www.catalystathletics.com/forum/showthread.php?t=4318)

When I was in an EKG class in college we spent some time in cardiac rehab and their workouts were about ten minutes of just rowing or basic running on treadmill. What kinds of issues are you having?

LSD activity builds thicker heart muscles, but that muscle is weak.

Heavy strength training builds stronger heart muscle without much hypertrophy.

The size of one's heart is not important when compared to the function of one's heart.

Your attempt to drop weight quickly most likely significantly negatively affected your mineral levels (aka electrolytes). The heart is a biochemical electrical machine, thus minerals are heavily implicated in rhythm disturbances, especially with those who try to sweat out bodyweight without replacing electrolytes that get depleted.
Update on the relationship between magnesium and exercise.

Quote:

Magnesium is involved in numerous processes that affect muscle function including oxygen uptake, energy production and electrolyte balance. Thus, the relationship between magnesium status and exercise has received significant research attention. This research has shown that exercise induces a redistribution of magnesium in the body to accommodate metabolic needs. There is evidence that marginal magnesium deficiency impairs exercise performance and amplifies the negative consequences of strenuous exercise (e.g., oxidative stress). Strenuous exercise apparently increases urinary and sweat losses that may increase magnesium requirements by 10-20%. Based on dietary surveys and recent human experiments, a magnesium intake less than 260 mg/day for male and 220 mg/day for female athletes may result in a magnesium-deficient status. Recent surveys also indicate that a significant number of individuals routinely have magnesium intakes that may result in a deficient status. Athletes participating in sports requiring weight control (e.g., wrestling, gymnastics) are apparently especially vulnerable to an inadequate magnesium status. Magnesium supplementation or increased dietary intake of magnesium will have beneficial effects on exercise performance in magnesium-deficient individuals. Magnesium supplementation of physically active individuals with adequate magnesium status has not been shown to enhance physical performance. An activity-linked RNI or RDA based on long-term balance data from well-controlled human experiments should be determined so that physically active individuals can ascertain whether they have a magnesium intake that may affect their performance or enhance their risk to adverse health consequences (e.g., immunosuppression, oxidative damage, arrhythmias).

I would suggest looking into these:
http://www.crayhonresearch.com/shop/...trate-p12.html
Particularly their "sports" version. If you aren't able to purchase them (they might only sell to practitioners) and you want them, PM me. Natural Calm plus Calcium would be a lesser option (it contains Ca, Mg, and K) in this situation. If it were me, I'd be supplementing my water all day long until the issue resolved.

I can only hope you learned from this experience.

Quote:

Iowa wrestling study: weight loss and urinary profiles of collegiate wrestlers.

A longitudinal study was conducted with various members of the 1975 University of Iowa NCAA championship wrestling team to determine if excessive weight loss, accompanied by signs of dehydration, occurred at the college level of competition. Body weight changes from September to December indicated a mean loss of 6%, while skinfold totals (6 sites) changed from a mean of 58 mm to 37 mm. During a four-month period, mean weight losses of 10.2, 9.5, 8.0, 7.5 and 7.0 lbs occurred in intervals of 12, 4, 3, 2 and 1 day, respectively. Basal urines analyzed throughout the season usually contained 2-3 times the potassium excreted before the season started. Analyses of urines at various intervals during a 2-day time period prior to weigh-in showed a .003 increase in specific gravity, 160 mosm/1 increase in osmolarity, .10 decrease in pH, 45.3 mEq/1 decrease in Na+ concentration, and a 71.3 mEq/1 increase in K+ concentration which suggested that the wrestlers were dehydrated prior to competition. Total urinary electrolyte loss during the 2 days amounted to 3.7% of estimated total body Na+ stores and 3.0% of total body K+ stores. These data were similar to what had been reported for Iowa high school finalists and indicated that collegiate wrestlers were also competing while in a dehydrated state.

Quote:

Applied physiology of amateur wrestling.

The general physiological profile of the successful wrestler is of one having high anaerobic power (mean range of 6.1 to 7.5 W/kg for arms; mean range of 11.5 to 19.9 W/kg for legs); high anaerobic capacity (range for arms 4.8 to 5.2 W/kg; range for legs 7.4 to 8.2 W/kg); high muscular endurance; average to above average aerobic power (range 52 to 63 ml/kg/min); average pulmonary function (range 1.90 to 2.02 L/kg/min for VEmax); normal flexibility; a high degree of leanness (range 3.7 to 13.0% fat) excluding heavyweights; and a somatotype that emphasises mesomorphy. Training methods include wrestling, and nonwrestling activities for increasing strength and power (i.e. resistance training), and to improve cardiovascular fitness (i.e. endurance training). Unfortunately, data on the isolated effects of wrestling on fitness and the type of training programme most effective for success in wrestling are scarce. The practice of weight loss is commonly used by wrestlers to enhance performance. Rapid weight loss has profound adverse effects on the wrestler's physiology but little effect on strength or anaerobic power performance as measured in the laboratory. In contrast, muscular endurance appears to be impaired by the rapid weight loss. Current research on weight loss and performance in wrestlers has taken 2 directions: (a) towards nutritional treatments to prevent suboptimal muscular endurance, and (b) towards the development of programmes to estimate minimal weight based on body composition techniques and thereby prevent weight reductions.

Quote:

Physiological effects of a weight loss regimen practiced by college wrestlers.

The effects of weight loss (dehydration) techniques (which mimicked techniques used prior to actual competition) used by intercollegiate wrestlers on selected physiological parameters (strength, anaerobic power, anaerobic capacity, the lactate threshold (LT), and peak aerobic power) were examined in seven intercollegiate wrestlers. During the 36 h weight loss period, subjects lost 3.3 kg (4.9% body weight), all of which occurred during the 12 h prior to weigh-in, using exercise in a rubberized sweat suit. Weight loss resulted in a reduction in upper body but not lower body strength measures (peak torque and average work per repetition). Anaerobic power and anaerobic capacity were significantly reduced in a dehydrated state (81.4 kgm.s-1, normal weight; 63.9 kgm.s-1, weight loss; 1984.3 kgm.40 s-1, normal weight; 1791.4 kgm.40 s-1, weight loss). Analyses of treadmill data revealed the following: 1) velocity was decreased at LT (4.4%) and peak (6.5%) during weight loss (P less than 0.05); 2) VO2 peak was significantly reduced with weight loss (6.7%, P less than 0.05); 3) treadmill time to exhaustion was significantly reduced in the weight loss state (12.4%) (35.7 min, normal weight; 31.3 min, weight loss). It was concluded that typical wrestling weight loss techniques result in deleterious effects on strength, anaerobic power, anaerobic capacity, the lactate threshold, and aerobic power.

I don't think I'll even consider "cutting weight" for OL. The potential damage just isn't worth it.

Also, I'd ditch the milk idea, if you're trying to have better heart health.

Quote:

Biological and Clinical Potential of a Palaeolithic Diet

Fat intake is not the only dietary factor that affects the atherosclerotic process in animal experiments. Many trials have shown that casein promotes atherosclerosis more than soy protein [43], and one trial suggested that meat proteins are less atherogenic than soy protein and casein [44]. Hence, meat may be less atherogenic than soy beans, low fat milk and high fat milk, in that order. The unfavourable impact of milk protein on serum cholesterol and atherosclerosis is commonly referred to as an effect of ‘animal protein’. However, the studies cited suggest that the term ‘animal protein’ is insufficiently specific and should be abandoned.

Quote:

Originally Posted by Andrew Wilson (Post 57665)

What kinds of issues are you having?

the other issue is that my liver is overactive. we're testing some other stuff to find out what's causing it. they think it's overaccumulation of fat sol. vitamins.

Garret - it's interesting you pointed out the ion issues. the doctors had never asked me about any of those factors or whether i had cut water before competitions. i've had some serious water weight drops before that have left me in a messed up mental state for a week afterwards. i think i was actually sodium deficient for a while too, as crazy as that may be. i'll bring it up at my next checkup.

another training question - what about negatives? i normally don't do negatives because i hate the DOMS when i try to grapple later, but i really haven't worked on negatives at all in a long time - mostly just dynamics and statics with some ME.

Quote:

Originally Posted by Grissim Connery (Post 57674)

Based on that history, you very likely have some pretty serious electrolyte deficiencies. This may or may not show up on typical bloodwork, and your conventional doc(s) may or may not believe that's the case. Your liver *must have* certain minerals to work correctly, that could also be connected to the same electrolyte deficiencies.

What kind of fat soluble vitamins are you taking and in what amounts? Unless you're taking a lot of vit. A, I don't think that's it.

As far as negatives go, all I can say is I'm personally trying to make negatives as small a portion of my workouts as possible (ie. dropping DLs from the top position, not lowering them).

i'm kinda back and forth about one of my doctor's respones to food. she seems both knowledgable in some areas and then she sometimes makes statements that i'm like "wtf, did she just say that?" i'm not the kinda guy to call somebody out in that situation, but i made mental notes. her and her assistant both seemed concerned when the IU's of my vitamins were in the thousands. i was thinking um yeah, that's not a big deal.

between a multivitamin and CLO:
D was about 1300 IU
A was about 19,000 IU

i doubt E or K affected me

now granted my food sources may have contributed more, but i don't always take my vitamins everyday, i was hardly consuming any dairy at that time, and i'm in cleveland (we literally just got sun). i doubt i passed the UL's with my food intake.

Quote:

Vitamin D toxicity, policy, and science.
Vieth R.

Departments of Nutritional Sciences, and Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.

The serum 25-hydroxyvitamin D [25(OH)D] concentration that is the threshold for vitamin D toxicity has not been established. Hypercalcemia is the hazard criterion for vitamin D. Past policy of the Institute of Medicine has set the tolerable upper intake level (UL) for vitamin D at 50 mug (2000 IU)/d, defining this as "the highest level of daily nutrient intake that is likely to pose no risks of adverse health effects to almost all individuals in the general population." However, because sunshine can provide an adult with vitamin D in an amount equivalent to daily oral consumption of 250 mug (10,000 IU)/d, this is intuitively a safe dose. The incremental consumption of 1 mug (40 IU)/day of vitamin D(3) raises serum 25(OH)D by approximately 1 nM (0.4 ng/ml). Therefore, if sun-deprived adults are to maintain serum 25(OH)D concentrations >75 nM (30 ng/ml), they will require an intake of more than the UL for vitamin D. The mechanisms that limit vitamin D safety are the capacity of circulating vitamin D-binding protein and the ability to suppress 25(OH)D-1-alpha-hydroxylase. Vitamin D causes hypercalcemia when the "free" concentration of 1,25-dihydroxyvitamin D is inappropriately high. This displacement of 1,25(OH)(2)D becomes excessive as plasma 25(OH)D concentrations become higher than at least 600 nM (240 ng/ml). Plasma concentrations of unmetabolized vitamin D during the first days after an acute, large dose of vitamin D can reach the micromolar range and cause acute symptoms. The clinical trial evidence shows that a prolonged intake of 250 mug (10,000 IU)/d of vitamin D(3) is likely to pose no risk of adverse effects in almost all individuals in the general population; this meets the criteria for a tolerable upper intake level.

Quote:

Safety of <7500 RE (<25000 IU) vitamin A daily in adults with retinitis pigmentosa.
Sibulesky L, Hayes KC, Pronczuk A, Weigel-DiFranco C, Rosner B, Berson EL.

Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA, USA.

BACKGROUND: Vitamin A supplementation is being used successfully to treat some forms of cancer and the degenerative eye disease retinitis pigmentosa. The daily biological need for vitamin A is estimated to be 800 retinol equivalents (RE)/d (2667 IU/d) for adult women and 1000 RE/d (3300 IU/d) for adult men; doses > or = 7500 RE (> or = 25000 IU)/d are considered potentially toxic over the long term. OBJECTIVE: We assessed the safety in adults of long-term vitamin A supplementation with doses above the daily biological need but <7500 RE (<25000 IU)/d. DESIGN: Adults aged 18-54 y with retinitis pigmentosa but in generally good health (n = 146) were supplemented with 4500 RE (15000 IU) vitamin A/d for < or = 12 y (group A) and compared with a similar group (n = 149) that received 23 RE (75 IU)/d (trace group). Mean total consumption of vitamin A in group A was 5583 RE (18609 IU)/d (range: 4911-7296 RE/d, or 16369-24318 IU/d) and that in the trace group was 1053 RE (3511 IU)/d (range: 401-3192 RE/d, or 1338-10638 IU/d). RESULTS: Patients in group A showed an 8% increase in mean serum retinol concentration at 5 y and an 18% increase at 12 y (P < 0.001); no retinol value exceeded the upper normal limit (3.49 micromol/L, or 100 microg/dL). Mean serum retinyl esters were elevated approximately 1.7-fold at 5 y and remained relatively stable thereafter. No clinical symptoms or signs of liver toxicity attributable to vitamin A excess were detected. CONCLUSIONS: Prolonged daily consumption of <7500 RE (<25000 IU) vitamin A/d can be considered safe in this age group.

The vit. D level is no concern, actually, you could likely double it if you wanted to (I would if I were you, especially living in Cleveland). See this article on how much D you can take: Am I Vitamin D Deficient?

The vit. A you are taking could absolutely be a part of the problem. I would suggest you take no more than 10000iu daily until this situation is resolved. Some people do not tolerate that much vit. A well at all.
http://www.westonaprice.org/basicnut...fications.html

The vit. A adjustment could easily take care of all the liver numbers. Go there first.